Salt appetite is a complex behavior that occurs under a variety of conditions, many of which are appropriate responses to real or perceived deficits of body sodium but some of which are not. As with other behaviors, interactions between peripheral and brain mechanisms are responsible for the presence, or absence, of salt appetite. In the brain it is now apparent that both excitatory and inhibitory components influence the expression of salt appetite. Studies from many laboratories have implicated several neuropeptides and several areas of the brain as potentially being involved in the control of salt appetite, but to date there is no consensus about the brain pathways essential for either excitation or inhibition of this behavior. Recent studies from our laboratories have shown that neuronal expression of the immediate early gene product Fos can identify neural pathways that are activated by a specific stimulus, and can differentiate these from pathways activated by related but nonetheless distinct stimuli. This methodology therefore enables an assessment of the brain circuits that are activated by stimuli that excite or inhibit specific behaviors under defined experimental conditions. The studies in this project utilize fos expression as a marker of neuronal activation after treatments known to excite or inhibit salt appetite in rats. Analysis of the stimulated patterns of Fos activation in response to multiple different treatments will allow identification of a common subset of brain areas that are activated in response to excitation or inhibition of salt appetite. Additional studies will pair excitatory and inhibitory treatments to ascertain the patterns of brain Fos activation under conditions of mixed stimuli that likely occur under physiological circumstances, and will compare the patterns of brain Fos activation in response to treatments that inhibit salt appetite to those accompanying physiological satiation of this appetite. Analysis of the neurochemical phenotypes and connectivity of the neurons activated to express Fos in response to treatments that either excite or inhibit salt appetite will allow analysis of the brain pathways involved in its control. These studies will therefore produce detailed descriptions of the brain areas that are essential for both excitation and inhibition of salt appetite in the rat, thereby defining the functional neuroanatomical basis of this important homeostatic behavior.